RESUMO
Blood pressure can be determined more precisely with the use of 24 hours ambulatory measurement in type 1 diabetics. Nitric oxide (NO) has been suggested to be responsible for the vascular changes described in early diabetic nephropathy. We aimed to investigate serum NO concentration along with ambulatory blood pressure monitoring (ABPM) parameters in type 1 diabetic patients and to find out whether there are correlation between serum NO level and ABPM parameters. Forty type 1 diabetic subjects and 35 controls were enrolled. Diabetic subjects were grouped as microalbuminuric (n=16) and normalbuminuric (n=24). Casual and ambulatory blood pressure parameters and serum NO concentrations were measured in all study population. Microalbuminuric subjects had higher nighttime systolic blood pressure (SBP), 24 hours diastolic blood pressure (DBP) and 24 hours mean arterial pressure (MAP) than controls. Both microalbuminuric and normalbuminuric subjects had also significantly higher nighttime DBP and nighttime MAP than controls. Serum NO concentrations were higher in normalbuminuric and microalbuminuric subjects than controls. Serum NO concentrations were positively correlated with daytime DBP and MAP, nighttime SBP, DBP and MAP, and 24 hours DBP and MAP in microalbuminuric subjects. Serum NO concentrations were also positively correlated with nighttime DBP in normalbuminuric subjects. Multiple linear regression analysis revealed that serum NO(2)- + NO(3)- concentrations and 24 hours DBP were independently associated with the development of microalbuminuria. Albuminuria seems to be closely associated with serum NO concentrations and ABPM parameters in type 1 DM patients. A prospective follow-up study on diabetic patients with normo- and micro- albuminuria is needed to confirm the predictive values of increased NO concentrations and ABPM parameters on the development of albuminuria.
Assuntos
Monitorização Ambulatorial da Pressão Arterial , Diabetes Mellitus Tipo 1/sangue , Diabetes Mellitus Tipo 1/fisiopatologia , Óxido Nítrico/sangue , Adolescente , Albuminúria/fisiopatologia , Criança , Feminino , Humanos , MasculinoAssuntos
Síndrome de Crigler-Najjar/genética , Glucuronosiltransferase/genética , Glucuronosiltransferase/metabolismo , Hiperbilirrubinemia Hereditária/genética , Mutação , Western Blotting , Criança , Síndrome de Crigler-Najjar/tratamento farmacológico , Regulação Enzimológica da Expressão Gênica , Vetores Genéticos , Humanos , Hiperbilirrubinemia Hereditária/tratamento farmacológico , Masculino , Fenobarbital/uso terapêuticoRESUMO
Congenital hypothyroidism (CH) is most commonly caused by defects in thyroid development leading to thyroid dysgenesis (80-90%), which consists of thyroid agenesis, ectopy or hypoplasia. Thyroid dysgenesis occurs mostly as a sporadic disease. However, a small but significant proportion of the cases are due to defects in transcription factors. The remaining 10-20% of congenital hypothyroidism is due to better-defined defects in any of the steps in the thyroid hormone biosynthesis, collectively called thyroid dyshormonogenesis, which are inherited autosomal recessively. Studying multiplex and/or consanguineous families with carefully defined, original phenotypes by such recently popular techniques as genome wide SNP genotyping with linkage search is likely to reveal novel disease associated genes. Thus there is new insight into the pathophysiology of congenital hypothyroidism.
